Vasovagal syncope is the commonest cause for syncope in our population.It is also referred to as simple syncope .The mechanism is thought to be an abnormal overshoot response by the vagus in response to a sudden surge of adrenegic activity usually occurring in erect posture following , often an emotional or physically stress full situation .The receptors for this reflex pathway is thought to be located left ventricular myocardium .

There are two components for the VV syncope

Cardio inhibitory

Vaso depressive.

The quantum of contribution by each component in a given episode of syncope varies. Pure vasodepressive or cardioinhibitory forms can occur .

Diagnostic issue

Before labeling a patient as simple vasovagal syncope all potentially serious , cardiac causes must be ruled out. this may require a fairly extensive investigation in some

Some will benefit from beta blockers, fludro cortisone(Increase the intra and extra cellular fluid space )

Since these are simple , cheap treatments , we worked over time to innovate & find some interventional solutions for this life threatening condition !!!. Thus , the indication for cardiac pacing for vasovagal syncope came into vogue .

DDDR pacemaker was implanted worldwide for thousands of patients with vasovagal syncope .

It took many years for our intellectual brains to realise , there are two limbs to vasovagal syncope Pacemakers , at no stretch of imagination is expected to counter vasodepresssive component of the syncope.

Water , (Simple H2O ! ) administered at right time in right quantity can prevent most episodes of vaso vagal syncope . When a tumbler of water can be substituted for a 10000 $ misadventure (DDD pacing) , and further we have hundreds of similar examples in modern day health care , no surprise why our health care system is sinking along with our economy !

Epilogue :

In this 21st century medical “AVATAR ” , we need to realise in a strong manner, low cost medicines often provide high quality cure ” while ,” many of the high cost therapies may end up in low quality treatment !

It took 50 years of intense research of medical comunity to realise , a good diet , physical activity and quitting smoking has the greatest way to control and reverse the cardiovascular epidemic . Please , note all of them come at free of cost .

Sinus node which orchestrtes the rhythm of life gets it’s blood supply by a small blood vessel arising from either RCA or LCX. (55 :45%) . The course of sinus node branch is highly variable .

There are three distinct pattern observed.

Posterior encircling of SVC .(50%)*

Anterior encircling of SVC(40%)

Form a “garland like ” anastomosis on either side of SVC (10%)

* Some refer to as clockwise and counterclockwise course.

SA node is a spindle shaped structure with a length up to 20mm . Extending from cranial to caudal aspect.The pecularity of the blood supply to SA nodal artery is , it enters the SA node either in it’s superior aspect or inferior aspect never in the mid part. There can be water shed area in the either ends depeding upon the entry.This can have electrophysiological and pathological significance .

The other consistent feature is that , the major trunk of SA node artery courses through the central core of SA node.In fact , many times pathologists recognise ther SA node , with the help of this arterial course.

Is there a collateral blood supply to SA node ?

It is not common . Rarely atrial branches of LCX /RCA can have extensive anastomosis with SA nodal branches .The hemodynamic significance of which is not known.

Ischemic SA nodal disease has become an important entity . As the cardiologists are preoccupied with opening occluded coronary arteries in cath labs , it is not surprising to note, there is little ongoing research in the anatomy and physiology of SA nodal blood supply.

We have to go back in time to get some great articles on the subject

At this point of time , we should realise the 1ooth anniversary of SA nodediscovery passed of silently . Kieth and Flack found the SA node with bare eyes in the year 1907 , when none of the present-day investigations including ECG and X RAY were not even conceptualised !

With tributes to those humble pathologists like M.J Davies, R.H .Anderson, T.N. James,M. Lev ,J.L.Titus who followed the foot steps of Kieth and Flack ,

Here is a link to one of the great articles on the blood supply to SA node

Related point : How do you recognise the SA nodal artery in coronary angiogram ?

During RCA angiogram it is many times confusing to identify the SA nodal branch . In RAO and LAO views the plane of exit of SA nodal branch from RCA will be determined by the course it is going to take .(Anterior vs posterior encircling pattern). The conal branch which is often the first branch of RCA , also behaves aberrantly many times. So, we can’t have a rule of thumb in identifying SA nodal branch .

When SA node branch originates from LCX it has to take a long route but once it reaches the SVC/RA junction it takes one of the above described course. It is not clear whether LCX fully understands it’s responsibility , when RCA ignores it 45 % of times . There is reason to suspect the commitment and dedication of LCX because it rarely supply the SA node by a seperate branch. It is often the left atrial CX that comes to the rescue and give a twig to the SA node .

Considering the complexity of SA nodal blood supply , one can understand why some develop premature sinus node failure. One can never determine with evidence , how much of SA node destruction is due to ischemia and how much is due to age related degeneration and fibrosis.

ASD is the most common acyanotic heart disease. Clinically distinguishing ostium primum (OP-ASD ) from ostium secundum (OS- ASD) is not an easy task . A Wide fixed split pf S2 , a short systolic murmur and PA pulsations in left second space, a loud P2 and a hyperdyanmic RV occur in both . The following features might give a clue for OP -ASD .

While OS-ASD is often an isolated anomaly , isolated OP- ASD is very rare.It usually occur as a part of partial or complete AV canal .

Early onset of symptoms

Early onset of pulmonary arterial hypertension( PAH )

Extra murmur of 1.VSD 2.MR (Cleft mitral valve ) may be present

Biventricular enlargement (MR/VSD)

ECG -Left axis deviation -Structural defect in left bundle ?

Confirmation is by Echocardiography and angiogram is rarely required today . Documentation of classical goose neck deformity of LV outflow confirms the diagnosis.

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Assessing LV function is the most common indication for doing echocardiography .Sinus tachycardia is the most common cardiac arrhythmia in humans. So, it is no surprise we encounter the above situation very often in echo labs.

The principle behind echo assessment of LV function is to measure the left ventricular wall thickening and the resultant reduction in LV cavity size.

The LV wall thickens in systole and returns to baseline thickness in diastole.When the heart rate increases the rate of thickening has to be faster, as do the rate of subsequent thinning in diastole. The endocardial segment of systole and thin segment of diastole tend to overlap at the base . borders are too shaggy and many times the thick So identifying true reference point for endocardium become a difficult task.

It is ironical , inspite of M mode echo being termed outdated and obsolete by most Echo schools , it remains the most utilized modality to measure LV function . It is highly unlikely , M-Mode derived LV EF will be replaced in the near future .This is because “simplicity will always prevail” over quality and accuracy .

It is all the more important , the already poor index of M-Mode – LV EF % becomes further error prone at high heart rates.

It need to be emphasised , the impact of tachycardia in confounding the true EF is greatest in patients with preexisting LV dysfunction .

In a normal heart the errors are less and it can be safely stated , tachycardias rarely result in clinically important LV function errors

To a certain extent , “yes ” . Here again the endocardial excursion is so fast one might have difficulty in marking the border.Automated border detection algorithms are never corrected for heart rate related errors.

Other issues in LV function assessment during tachycardia

In the presence of CAD , the coronary arteries often have varying degrees of obstruction. Hence ,the myocardial segments also exist in varying degrees of ischemia.

In patients with significant CAD ,tachycardia due to any cause (Compensatory /Non compensatory -Fever, anxiety etc) can be considered a stress to myocardium . (By all means , can we consider it an equivalent of dobutamine stress echo! ?)

We know , dobutamine stress echo , has a variable effect on the contractility of LV. It can either depress , argument, or have neutral effect .Different lesions have different response depending upon the baseline viability of myocardium . For example a 70% lesion subtending a infarcted – viable segment may improve , while a 90% lesion supplying a normal LV segment may either worsen or hypercontractile .

What is poor man’s viabilty test ?

Grossly differing LV EF % in two different echocardiograms at two different heart rates may be an indirect clue for the presence of viable myocardium.(Poor man’s PET or Thallium !)

The final message

The above concepts remind us the complexity of measuring the true EF in the presence of CAD. Purists, may even question the existence of a ” true normal EF” in a given patient

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T waves are the most enigmatic waves in clinical electrocardiography . This is not a surprise , when you consider a tall T wave and a markedly inverted T wave both can be normal in at least in 6 leads out of 12 lead standard electrocardiogram ( V1 V2 V3 , 2 ,3 AVF, ofcourse the AVR )

Common T wave patterns that can either be physiological or pathological

Tall T wave

Inverted T WAVE

Notched or Bifid T wave

Biphasic T wave

* T wave polarity is strongly determined by the direction of QRS vector. Generally it should be on the same direction as QRS. In the presence of conduction defect or chamber hypertrophy this gets altered and is refered toa s secondary repolarisation changes . This has to be differentiated from primary biphasic T waves.

What is a biphasic T wave ?

A T wave which is inscribed on either side of baseline is called biphasic T wave .

Many of the normal persons can have a biphasic Twave.

A typical biphasic wave can be two types

Terminal positivity

Terminal negativity

Terminal negativity is more significant than terminal positivity , especially in CAD.

Exercise stress testing(EST) is one of the common investigation modality in the evaluation of CAD.he indication for EST generally fall into two broad categories.

Diagnostic in patients suspected to have CAD

Prognostic evaluation in patients with established CAD .9Many times after a coronary angiogram)

Currently there is a major shift in our thinking, patients with classical angina may undergo coronary angiogram directly .This is understandable as the stress test has little to improve diagnostic sensitivity and specificity in patents with clinically obvious CAD.

So , it is now becoming clear , the diagnostic value is increasingly restricted in the evaluation of o atypical chest pain .

What is a strongly positive response ?

Gross ST segment depression > 2-3mm

Occurring in stage one

Fall in blood pressure

Prolonged angina into recovery

What is the angiographic correlates of strongly positive EST?

Critical left main disease

Near total proximal LAD /LCX

A severely compromised bifurcation lesion

Morphological correlation

These patients often have eccentric lesions with irregular margins.

unstable lesions

Lack collaterals

What is the effect of vigorous excercise on a critical flow limiting lesion ?

The shear stress over the plaque increases with exercise and the transcoronary gradient can reach a theoretical 60-90mmhg .One can imagine the what this stress can do to the unstable lipid core .This is the reason unstable angina is an absolute contraindication to EST.

What does a strongly positive EST imply for the patient ?

It indicates he needs urgent CAG and most likely an immediate revascularisation.

Often , these patients have prolonged angina , and mandates admission in a coronary care unit.

there has been many incidence of ACS in these patients within 24hours of EST.

Lives have been lost on their way back , as these patients are sent home , as EST is a OP procedure .

Final message

It need to be realised a strongly positive response to EST could be a clinical equivalent of unstable angina .

The common response from a physician or cardiologist after witnessing a gross ST depression to EST would be “Had I known this I would have sent him straight into cathlab instead of EST ”

If only , we give little ear to our patient’s history we can pick the high risk clue in 9 out of 10 cases !

It can be argued , a strongly positive EST by itself is “A clinical diagnostic failure” , ie failure of the physician to recognise the likely hood of strongly positive EST ie a left main disease.

These patients should never be sent home immediately after the EST .This is fraught with a risk SCD

Most of them will require observation in step down unit for 24 hours and if feasible they should be posted for coronary angiogram in the earliest available slot.